Experiments have been completed which suggest that the mixed function oxidase system in involved in the metabolism of 3-methylindole (3MI) and that this metabolism is also responsible for the pulmonary toxicity of this compound. The microsomal fraction of lung tissue retains more radioactivity from 14C-3MI than other subcellular fractions and the severity of pulmonary lesions can be altered by prior administration of inducers and inhibitors of the mixed function oxidase system. Electron microscope observations demonstrate cytotoxic alterations in specific types of lung cells within 1/2 hour after 3MI administration. These changes include swelling of cytoplasmic vesicles, mitochondria and other subcellular structures in aveolar Type I cells. In addition, there is proliferation of smooth endoplasmic reticulum in surviving cells. In other experiments, we have shown that various antibiotics and inhibitors are effective in reducing 3MI formation in ruminal fluid both in vitro and in vivo. This reduction in 3MI formation in the rumen of cattle given tryptophan prevents the onset of acute pulmonary lesions in these animals. These results are being used to establish the specific mechanism of action of 3MI as a model of chemically-induced lung disease and to develop a pratical means of prevention of naturally-occurring acute bovine pulmonary edema and emphysema.